Background and Aims: Learning and memory impairments are among the most frequent behavioral outcomes in patients with temporal lobe epilepsy (TLE). It has been well documented that the hippocampus, as the main structure of the temporal lobe, has a crucial role in learning and memory processes. Further, the hippocampus is principally involved in recurrent spontaneous seizures originating from the temporal lobe. Accumulating data indicates that progressive neurodegeneration in different parts of the hippocampus following prolonged seizure activities correlates with impairment in learning and memory performance. Common antiepileptic drugs are associated with a wide variety of side effects and worsening cognitive and memory disorders in TLE. Alpha-pinene (APN) is an essential oil belonging to the terpenoid family with multiple beneficial effects, including antioxidative, anti-inflammatory antiapoptotic, sedative, and anxiolytic properties. Therefore, we aimed to evaluate the possible therapeutic effects of APN in KA-induced memory decline in rats. We also examined the role of BDNF/TrkB/CREB signaling pathways in the hippocampus as an underpinning mechanism of APN pretreatment. Method: Male Wistar rats were used. APN (50 mg/kg/day) was administrated intraperitoneally for 14 days before induction of TLE using the intracerebroventricular injection of kainic acid (KA). Spatial working memory and inhibitory avoidance memory were assessed by using Y-maze and inhibitory avoidance tests, respectively. Neuronal loss in the CA1 region of the hippocampus was also evaluated with Nissl staining. The protein levels of BDNF, TrkB, and CREB were examined by a western blotting method using appropriate antibodies. Results: The results indicated that APN pretreatment had preventive effects against KA-induced memory deficit and significantly increased survival of the CA1 neurons. The western blotting analysis demonstrated that the protein levels of BDNF, TrkB, and CREB in the hippocampus upregulated in response to APN pretreatment. Conclusion: It can be concluded that APN acts as a neuroprotective agent and ameliorates memory impairment through the restoration of BDNF/TrkB/CREB signaling pathways in the rat hippocampus in a KA-induced TLE model.
